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Beneficial effects of melatonin in experimental models of Alzheimer disease

Acta Pharmacologica Sinica 2006年第2期27卷 129-139页

作者： Yong CHENG~2 Zheng FENG~3 Qing-zhu ZHANG~4 Jun-tian ZHANG~(2.5) ~2Department of Pharmacology,Institute of Materia Medica,Chinese Academy of Medical Sciences and Peking Union Medical College,Beijing 100050,China:~3Department of Anesthesiology,University of California,San Diego,and Veterans Affairs Medical Center,3350 La Jolla Village Drive,San Diego,CA 92161,USA:~4Department of Pharmacology,College of Pharmacy,Shandong University,Jinan 250012,China InstituteofMateriaMedica ChineseAcademyofMedicalSciencesandPUMCBeijing100050China DepartmentofAnesthesiology UniversityofCaliforniaSanDiegoandVeteransAffairsMedicalCenterUSA CollegeofPharmacy ShandongUniversity

Alzheimer’s disease(AD),a progressive degenerative disorder,is characterizedby the presence of amyloid deposits,neurofibrillary tangles and neuron *** evidence indicates that antioxidants could be useful either for the pre-vention or treatment of *** has been shown that melatonin is a potent antioxi-dant and free radical ***,melatonin stimulates severalantioxidative enzymes and improves mitochondrial energy *** find-ings led us to study amyloid precursor protein transgenic mice,ovariectomizedrats,and pheochromocytoma and astroglioma cell lines,to observe whether mela-tonin had any effect on Alzheimer’s symptoms or pathological *** foundthat melatonin had many beneficial effects in experimental models of AD,includ-ing improvement of cognitive function,anti-oxidative injury,anti-apoptosis,inhi-bition of β-amyloid(Aβ)deposition and Aβ fiber *** groups haveshown that melatonin has an inhibitory effect on tau protein *** actions may potentially slow down or stop the progression of dementia.

关键词： melatonin Alzheimer disease beta-amyloid protein calcium overload app transgenic mice ovariectomized rats tau protein hyperphosphorylation

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Deficit of learning memory ability and increased expression of α-synuclein with aging in app transgenic model of Alzheimer disease

Deficit of learning memory ability and increased expression ...

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中国神经科学学会第六届学术会议暨学会成立十周年庆祝大会

作者： Zhang Lan, Li Lin, Yu Shun, Xing Ying, Ye Cui-fei, Li Yao-hua, Chen Biao Dept. Phannacology, Dept. Neurobiology, Xuan-wu hosp of Capital University of Medical Sciences, Beijing Key Laboratory for Brain Aging, Beijing 100053, China

＜正＞Objective: α-synuclein was identified on the basis of proteolytic fragments derived from senile plaques of Alzheimer disease （AD）. It’s unknown whether synucleins may play an important role in neural degeneration. The aim of the present study was to investigate learning-memory deficit and the expression change of α-synuclein in the brain of AD-like animal model at different age and to explore the pathology mechanism of α-synuclein in neural degeneration. Methods: app V717I transgenic （Tg） mice model of Alzheimer’s disease was observed at age of 4 month ,10 month and 16 month old. The Tg mice were randomly divided into 3 model groups （4 month, 10 month and 16 month old） , Control adapted the same age and background C57BL/6J mice. Learning-memory ability was detected by Morris water maze and object recognition test. The mRNA expression of α-synuclein was measured by genechips and RT-PCR method. The protein production of α-synuclein was detected by immuno- histochemistry and western blotting. A generally accepted animal model. Results: For 4 month old app Tg mice,

关键词： Alzheimer disease (AD) app transgenic mice a-synuclein learning-memory ability

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